Browse our Ret Proto-Oncogene Proteins (RET)

Zebrafish Ret Proto-Oncogene (RET) interaction partners

1. Authors observed no interaction between efn-A5b and RET from zebrafish, this lack of association indicates how complex efn-A signaling is and suggests that there may be other molecules involved in efn-A5-induced RET signaling.

2. These data provide the first evidence for a physiologic role of these isoforms in RET pathway function.

3. Significantly, we show that introduction of mapk10 mutations into ret heterozygotes enhanced the ENS deficit, supporting MAPK10 as a Hirschsprung disease (HSCR) susceptibility locus. Our studies demonstrate that ret heterozygous zebrafish is a sensitized model, with many significant advantages over existing murine models, to explore the pathophysiology and complex genetics of HSCR.

4. RET expression is investigated within the brain of zebrafish; both RET protein and mRNA are observed.

5. In animals lacking Ret or Gfra3 function, myogenic gene expression is reduced in forming opercular muscles, but not in non-opercular muscles derived from the same muscle anlagen.

6. evaluation of noncoding sequences at the zebrafish ret locus conserved among teleosts, and at the human RET locus, conserved among mammals

7. genes beyond RET may be implicated in the genesis of sporadic cases of HD

Human Ret Proto-Oncogene (RET) interaction partners

1. we detected RET gene rearrangements in 384 patients with advanced primary NSCLC by RT-PCR and found a RET gene rearrangement rate of 1.82%. We also found a higher prevalence of RET gene rearrangements in primary compared with metastatic lesions (chi2=91.117, P<0.001). The presence of RET rearrangement in the primary tumor could be predicted by rearrangement in the corresponding metastatic lesion (kappa=0.798, P<0.001)

2. mutation was found in 23.8% of hereditary medullary thyroid carcinoma patients tested; most commonly mutated codon was codon 634 (37.1%), followed by codon 918 (14.3%)

3. Novel low frequency SNP in ERT locus is associated with Hirschsprung disease.

4. RET alterations, such as RET-oncogene fusions, are present in a subset of breast cancers, and are promising therapeutic targets.

5. RET gene alterations (copy number gain and rearrangement) exist in all RET-positive samples. RET-positive expression is a relatively independent factor in non-small cell lung cancer cases(NSCLC) patients, which indicates that the RET gene may be a novel target site for personalized treatment of NSCLC.

6. Somatic mutations of the RET gene are underrecognized in HSCR. Molecular investigation of the parents of patients with seemingly sporadic mutations is essential to determine recurrence risk in these families.

7. in vitro transactivation of the RET promoter by different Hirschsprung disease-associated PHOX2B polyA variants has resulted significantly lower compared to the effect of PHOX2B wild type protein.

8. These results support the association between genetic variation of RET and NRG1 and susceptibility to Hirschsprung disease in the Chinese population.

9. the results from three transcriptome-based platforms (Nanostring Elements, Agena LungFusion panel and ThermoFisher NGS fusion panel) were compared to those obtained from ALK, ROS1 and RET Fluorescence In Situ Hybridization on 51 clinical specimens.

10. The authors found a significant association between the localization of RET mutations and the expression of three genes: NNAT (suggested to be a tumour suppressor gene), CDC14B (involved in cell cycle control) and NTRK3 (tyrosine receptor kinase that undergoes rearrangement in papillary thyroid cancer) in patients with medullary thyroid cancer.

11. the inverse relationship between GFRalpha1 and C-Ret, as knocking down C-Ret led to increases in GFRalpha1 expression.

12. Rare synonymous changes in the RET gene, c.1827C>T (p.Cys609Cys), c.2364C>T (p.Ile788Ile), and c.2673G>A (p.Ser891Ser), were identified in medullary thyroid carcinoma patients and c.2418C>T (p.Tyr806Tyr) in a patient suspected of MEN2 syndrome

13. RET rearrangement is associated with lung adenocarcinoma.

14. The data suggest that all families with the C611Y germline mutation in Denmark originate from a recent common ancestor, probably explaining the unusually high prevalence of this mutation in Multiple Endocrine Neoplasia 2A families.

15. Our results demonstrated greater expression of pRET and CXCR4 in cisplatinresistant neuroblastomas (NBs). Vandetanib significantly inhibited SHSY5YR cell proliferation, colony formation, and invasion, while downregulating pRET and CXCR4 expression

16. LRIG1 is a negative regulator of RET2A and RET2B and is also downregulated in papillary and medullary thyroid carcinoma

17. Study in SK-N-MC cells found that C634R mutation could enhance RET protein expression and change the location of the mutated protein and forced it into the nucleus.

18. The frequencies of ALK, ROS1 and RET rearrangements are low in non-adenocarcinoma NSCLC patients. And their clinical characteristics are similar to those in lung adenocarcinoma. Fusions of the above 3 genes are not prognostic factor for non-adnocarcinoma NSCLC patients.

19. BRAFV600E and RET/PTC and the expression of NF-kappaB promote the proliferation and migration of papillary thyroid carcinoma cells in vitro.

20. The RET proto-oncogene located on chromosome 10q11.2 encodes a 1114-amino acid transmembrane receptor with a cadherin-related motif and a cysteine-rich domain in the extracellular domain.

Mouse (Murine) Ret Proto-Oncogene (RET) interaction partners

1. p75 is required for the development of the nonpeptidergic nociceptor lineage by fine-tuning Ret-mediated trophic support.

2. 7-DHC efficiently supports Ret signaling in vitro.

3. Results showed that Mn-mediated age-related hearing loss involved a decreased expression and phosphorylation levels of c-Ret in spiral ganglion neurons.

4. Compromised Survival of Cerebellar Molecular Layer Interneurons Lacking GDNF Receptors GFRalpha1 or RET Impairs Normal Cerebellar Motor Learning

5. Data show that NEDL2 regulates GDNF/Ret/Akt pathway depends on its Nedd8 ligase activity rather than ubiquitin ligase activity.

6. The cardiac GFRA2 signaling pathway is distinct from the canonical pathway dependent on the RET tyrosine kinase.

7. Ret is essential to mediate GDNF's neuroprotective and neuroregenerative effect in a Parkinson disease mouse model.

8. Mechanistically, Ret is engaged in a positive feedback loop with Wnt/Wingless signalling, modulated by Src and Fak kinases.

9. Authors did not find evidence for genetic interaction between Ret and Sema3d affecting survival, presence of myenteric plexus or intestine transcriptome.

10. findings uncover a novel spinal circuit that mediates crosstalk between touch and pain pathways and suggest that some early RET positive Dorsal Horn neurons could function as pain "gating" neurons.

11. Using an organ culture system for prostate development and Ret mutant mice, we demonstrate that RET-mediated GDNF signaling in UGS increases proliferation of mesenchyme cells and suppresses androgen-induced proliferation and differentiation of prostate epithelial cells, inhibiting prostate development.

12. we described a RET-ER81-Neuregulin1 signaling pathway in neurons innervating Pacinian corpuscle somatosensory end organs, which is essential for communication between the innervating axon and the end organ

13. These data provide the first evidence for a physiologic role of these isoforms in RET pathway function.

14. Hox proteins coordinate motor neuron differentiation and connectivity programs through Ret/Gfra genes.

15. Ret and Gfra2 null mice display comparable early central projection deficits, but Gfra2 null rapidly adapting mechanoreceptors recover later.

16. Parkin and the RET signaling cascade converge to control mitochondrial integrity and thereby properly maintain substantia nigra pars compacta dopaminergic neurons and their innervation in the striatum.

17. the Ret signaling pathway is important for podocyte survival and recovery from glomerular injury in vivo

18. RET coupling to ERK and Akt depends strongly on artemin concentration, and it is highest at the low (~100 pM) artemin levels required for neurite outgrowth.

19. we analysed non-thermal, atmospheric pressure, plasma irradiation mediated effects in melanocytic tumors which spontaneously developed in HL-RET-mice

20. the important IL-10 transcription factor Maf was upregulated in RET-deficient Th2 cells and down-regulated upon RET signalling activation by glial-derived neurotrophic factor family ligands.